A dominant-interfering camta3 mutation compromises primary transcriptional outputs mediated by both cell surface and intracellular immune receptors in Arabidopsis thaliana.

Abstract

Summary Pattern recognition receptors (PRRs) and nucleotide‐binding domain and leucine‐rich repeat (LRR)‐containing proteins (NLRs) initiate pattern‐triggered immunity (PTI) and effector‐triggered immunity (ETI), respectively, each associated with the activation of an overlapping set of defence genes. The regulatory mechanism behind this convergence of PTI‐ and ETI‐mediated defence gene induction remains elusive.We generated transgenic Arabidopsis plants that enable conditional NLR activation without pathogen infection to dissect NLR‐ and PRR‐mediated transcriptional signals. A comparative analysis of over 40 transcriptome datasets linked calmodulin‐binding transcription activators (CAMTAs) to the activation of overlapping defence genes in PTI and ETI. We used a dominant camta3 mutant (camta3‐D) to assess CAMTA functions in the corresponding transcriptional regulation.Transcriptional regulation by NLRs, although highly similar to PTI responses, can be established independently of pathogen‐associated molecular pattern (PAMP) perception, defence phytohormones and host cell death. Conditional expression of the N‐terminal coiled‐coil domain of the barley MLA (Mildew resistance locus A) NLR is sufficient to trigger similar transcriptional reprogramming as full‐length NLRs. CAMTA‐binding motifs are overrepresented in the 5′ regulatory regions of the identified primary immune response genes, consistent with their altered expression and disease resistance responses in camta3‐D plants.We propose that CAMTA‐mediated transcriptional regulation defines an early convergence point in NLR‐ and PRR‐mediated signalling.